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  1. NTU Theses and Dissertations Repository
  2. 醫學院
  3. 醫學檢驗暨生物技術學系
請用此 Handle URI 來引用此文件: http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/32414
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dc.contributor.advisor楊雅倩
dc.contributor.authorSheng-Tai Tzengen
dc.contributor.author曾晟泰zh_TW
dc.date.accessioned2021-06-13T03:47:57Z-
dc.date.available2010-08-02
dc.date.copyright2006-08-02
dc.date.issued2006
dc.date.submitted2006-07-26
dc.identifier.citation1. http://tpmd.nhri.org.tw/php-bin/index_en.php.
2. http://www.doh.gov.tw/statistic/index.htm.
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12. Hammoud, Z. T., Z. Kaleem, J. D. Cooper, R. S. Sundaresan, G. A. Patterson, and P. J. Goodfellow. 1996. Allelotype analysis of esophageal adenocarcinomas: evidence for the involvement of sequences on the long arm of chromosome 4. Cancer Res 56:4499-502.
13. Kern, S. E., E. R. Fearon, K. W. Tersmette, J. P. Enterline, M. Leppert, Y. Nakamura, R. White, B. Vogelstein, and S. R. Hamilton. 1989. Clinical and pathological associations with allelic loss in colorectal carcinoma [corrected]. Jama 261:3099-103.
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15. Loughran, O., L. J. Clark, J. Bond, A. Baker, I. J. Berry, K. G. Edington, I. S. Ly, R. Simmons, R. Haw, D. M. Black, R. F. Newbold, and E. K. Parkinson. 1997. Evidence for the inactivation of multiple replicative lifespan genes in immortal human squamous cell carcinoma keratinocytes. Oncogene 14:1955-64.
16. Meijer, G. A., M. A. Hermsen, J. P. Baak, P. J. van Diest, S. G. Meuwissen, J. A. Belien, J. M. Hoovers, H. Joenje, P. J. Snijders, and J. M. Walboomers. 1998. Progression from colorectal adenoma to carcinoma is associated with non-random chromosomal gains as detected by comparative genomic hybridisation. J Clin Pathol 51:901-9.
17. Paredes-Zaglul, A., J. J. Kang, Y. P. Essig, W. Mao, R. Irby, M. Wloch, and T. J. Yeatman. 1998. Analysis of colorectal cancer by comparative genomic hybridization: evidence for induction of the metastatic phenotype by loss of tumor suppressor genes. Clin Cancer Res 4:879-86.
18. Pershouse, M. A., A. K. El-Naggar, K. Hurr, H. Lin, W. K. Yung, and P. A. Steck. 1997. Deletion mapping of chromosome 4 in head and neck squamous cell carcinoma. Oncogene 14:369-73.
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21. Ried, T., R. Knutzen, R. Steinbeck, H. Blegen, E. Schrock, K. Heselmeyer, S. du Manoir, and G. Auer. 1996. Comparative genomic hybridization reveals a specific pattern of chromosomal gains and losses during the genesis of colorectal tumors. Genes Chromosomes Cancer 15:234-45.
22. Roth, S., M. Johansson, A. Loukola, P. Peltomaki, H. Jarvinen, J. P. Mecklin, and L. A. Aaltonen. 2000. Mutation analysis of SMAD2, SMAD3, and SMAD4 genes in hereditary non-polyposis colorectal. J Med Genet 37:298-300.
23. Schimanski, C. C., G. Schmitz, A. Kashyap, A. K. Bosserhoff, F. Bataille, S. C. Schafer, H. A. Lehr, M. R. Berger, P. R. Galle, S. Strand, and D. Strand. 2005. Reduced expression of Hugl-1, the human homologue of Drosophila tumour suppressor gene lgl, contributes to progression of colorectal cancer. Oncogene 24:3100-9.
24. Shivapurkar, N., A. Maitra, S. Milchgrub, and A. F. Gazdar. 2001. Deletions of chromosome 4 occur early during the pathogenesis of colorectal carcinoma. Hum Pathol 32:169-77.
25. Shivapurkar, N., S. Sood, Wistuba, II, A. K. Virmani, A. Maitra, S. Milchgrub, J. D. Minna, and A. F. Gazdar. 1999. Multiple regions of chromosome 4 demonstrating allelic losses in breast carcinomas. Cancer Res 59:3576-80.
26. Shivapurkar, N., A. K. Virmani, Wistuba, II, S. Milchgrub, B. Mackay, J. D. Minna, and A. F. Gazdar. 1999. Deletions of chromosome 4 at multiple sites are frequent in malignant mesothelioma and small cell lung carcinoma. Clin Cancer Res 5:17-23.
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dc.identifier.urihttp://tdr.lib.ntu.edu.tw/jspui/handle/123456789/32414-
dc.description.abstract大腸直腸癌全球每年有超過875,000個病例被報告,近年來並在台灣地區十大癌症死因中排名第三。大部分的大腸直腸癌源自於黏膜上皮細胞的增生,慢慢累積形成良性的瘜肉或腺瘤,再經過一段時間轉變成惡性的癌細胞,由於基因變異的累積需要時間,因此患者也以中老年人為主。最近的研究報告指出,大腸直腸腫瘤在染色體4、8p、17p和18q最常發生染色體漏失的現象,而這些染色體變化與癌症進展、病人存活時間及腫瘤轉移亦有相關,意味著這些染色體區域極可能存在著與大腸直腸癌相關的腫瘤抑制基因。在本實驗室先期的研究中,利用分布在第四號染色體上的22個微衛星標記,針對106例大腸直腸腫瘤進行失異合性 (loss of heterozygosity,LOH) 分析,結果發現了三個發生LOH頻率較高的標記,分別是D4S2964、D4S402及D4S413,其中又以D4S402 (4q27) 基因座發生率最高,為32.9%;而此位點與鄰近的兩個標記D4S406及D4S1575的距離各為7.4及9.5 cM。為了在此約長17 cM區域尋找與大腸直腸癌相關的腫瘤抑制基因,必須進一步定出更小範圍的刪除區域,本論文選擇在D4S402附近 (4q25-4q28.2) 再以十個微衛星標記進行分析,每個微衛星標記之間相隔距離縮小為1~2cM,以繼續建構大腸直腸癌位於染色體4q25-4q28.2區域的高解度刪除圖譜。以70例不同癌症分期的大腸直腸癌檢體,利用螢光標記的引子進行微衛星擴增反應,再藉由毛細管電泳進行分析。結果發現41.4%的案例有LOH變化,而LOH發生率最高的位點為位於4q26的D4S2303 (26.8%),並藉此定出4q25-4q28.2一段最常發生刪除的區域(位於第四號染色體118.5~119.8 cM)。我們也將此區域刪除的情形與病人臨床資料做統計分析,發現癌症後期於此區域的刪除發生率由初期的15%上升到40% (P=0.031)。這些結果支持在第四號染色體此區域存在與大腸直腸癌相關的腫瘤抑制基因的假設。論文中也針對118.5~119.8 cM區域內的UGT8 (UDP glycosyltransferase 8) 基因,利用反轉錄-聚合酶連鎖反應的方法做初步的基因表現分析。zh_TW
dc.description.provenanceMade available in DSpace on 2021-06-13T03:47:57Z (GMT). No. of bitstreams: 1
ntu-95-R93424006-1.pdf: 1322029 bytes, checksum: 62f96c9843e3d8ccd9c98a5e918e2eb8 (MD5)
Previous issue date: 2006
en
dc.description.tableofcontents目錄
誌謝 i
中文摘要 ii
英文摘要 iii
第一章 導論 1
1.1 大腸直腸癌簡介 1
1.2 微衛星標記簡介 6
1.3 研究背景與目的 7
第二章 材料與方法 9
2.1 實驗材料 9
2.2 抽取組織DNA 10
2.3 微衛星標記分析 10
2.4 抽取組織RNA 11
2.5 細胞株培養 12
2.6 基因表現實驗 12
2.7 LOH與臨床資料統計 13
第三章 結果 14
3.1 微衛星標記之PCR反應與毛細管電泳 14
3.2 大腸直腸癌組織的分析結果 14
3.3 大腸直腸癌腫瘤臨床資料與LOH的統計分析 15
3.4 座落於第四號染色體高度刪除區域Region I (118.5-119.8 cM)的基因 15
3.5 UGT8基因於大腸直腸癌組織的表現 16
第四章 討論 18
圖 21
表 32
參考文獻 42
附錄一:附錄表格 45
附錄二:實驗步驟 50
dc.language.isozh-TW
dc.title大腸直腸癌位於染色體4q25-4q28.2之高解度刪除圖譜繪製zh_TW
dc.titleHigh-resolution Mapping of Allelic Loss at Chromosome 4q25-4q28.2 in Colorectal Carcinomaen
dc.typeThesis
dc.date.schoolyear94-2
dc.description.degree碩士
dc.contributor.oralexamcommittee蔡明宏,俞松良,方偉宏
dc.subject.keyword大腸直腸癌,刪除圖譜,zh_TW
dc.subject.keywordcolorectal carcinoma,mapping,en
dc.relation.page67
dc.rights.note有償授權
dc.date.accepted2006-07-26
dc.contributor.author-college醫學院zh_TW
dc.contributor.author-dept醫學檢驗暨生物技術學研究所zh_TW
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